A major objective of my research is to obtain a better understanding of the biochemical mechanisms which are responsible for the loss in muscle mass occurring during periods of physical inactivity. I have previously reported that muscle disuse results in decreases in muscle size and in the quantity of mitochondria. I now aim to determine in muscle undergoing disuse atrophy whether the decreases in the pool sizes of cytochrome c, myoglobin, and myosin and the increase in collagen concentration are due to changes in the synthesis rate in the degradation rate or of both rates. Another of my aims will be to discover which of the acute changes in cellular homeostasis of muscle (that is associated with physical inactivity) is responsible for the loss of muscle protein. I have also previously reported that there is a preferential loss of slow-twitch (or anti-gravity) muscle fibers during disuse atrophy. Moreover, there is an increase in the concentrations of collagen and calcium in atrophying muscle. There are preliminary reports suggesting that slow-twitch muscles may not recover to their pre-atrophy weights. A third aim will be to determine whether these changes are reversed during rehabilitation and whether slow-twitch muscles ever regain pre-atrophy levels. A fourth major objective is to determine whether the increase in rate of synthesis, the decrease in the rate of degradation, or both are playing the major role in the adaptive increase in the total pool sizes of cytochrome c, myoglobin, and myosin during the rehabilitative growth of atrophied muscle. Another objective of this proposal is to gain information on the sequence of biochemical events resulting from the increase in the amount of contractile activity in muscles after immobilization, and leading to the rehabilitative growth of the muscle.